EPM Flashcards
how is EPM transmitted?
Sarcocystic neurona is ingested by the intermediate hosts (cats, armadillos, skunks, etc.) that develop sarcocysts in the muscle that is then eaten by the definitive hosts, opossums. The opossums have bradyzoites released into the GI tract that become sporulated oocytes which is then excreted in the feces. Then horses eat the feces or contaminated water,etc. and are infected in the brain and spinal cord with schizonts and merozoites being ID’d.
what is the prevalence of EPM and how is it transmitted?
seroprevalence of sarcocystis neurona is high but disease prevalence is low (1% develop disease)
what factors influence development of disease in an individual animal with EPM?
Dose, stress, season, strain and immune response
what are the common clinical signs of EPM?
Ataxia
Asymmetric
Atrophy
top differential for multifocal CNS disease and most frequently slowly progressive
what three steps should be taken in diagnosing EPM?
- Confirm the presence of clinical signs that are consistent with EPM (complete neuro exam)
- Rule out other diseases (lameness, CBC/Chem, serology, Rads, CSF cytology)
- Confirm intrathecal antibody production through immunodiagnostic testing on serum and CSF (western blot, ELISA, IFAT)
what diagnostic tests are available and what are their limitations for EPM?
- Serum testing for antibodies: This is only valuable if the horse is negative since the majority of horses have been exposed and will be positive (low positive predictive value but high negative predictive value). The only exception is if the horse is very early in disease.
- CSF antibodies: more informative but still causes fake positives. Ratio of serum to CSF reflects intrathecal production and is the best way to dx pre mortem
what treatments are available for EPM?
Antiprotozoal drugs such as rebalance, ponazuril (marquis) and diclazuril (protazil) with supportive medical treatment
what is the prognosis for horses with EPM?
remove opossums, dont feed from the ground, fence out underbrush and give ponazuril and diclazuril
T/F: CSF for a horse with EPM is almost always normal
T
T/F: hematology and serum biochemistry of a horse with EPM is usually normal
T
T/F: there is a gold standard diagnostic tool for EPM
F
IFAT
Gives titers and probabilities of active infection but there is little correlation with active infections . It can be used to calculate a serum: CSF ratio
SAG 1 ELISA has a __ sensitivity since not all pathogenic strains of S. neurona express the antigen.
SAG 1 ELISA has a low sensitivity since not all pathogenic strains of S. neurona express the antigen.
SnSAG2 ELISA and the SnSAG4/3 ELISA
These were shown to be the most consistently expressed antigens across isolates with the ratio of serum: CSP being predicative of EPM
T/F: testing serum alone is reliable when testing for EPM
F, low specificity
Neospora hughesis diagnosis
There aren’t alot of cases but you can run either a NhSAG 1 or IFAT test if others tests come back negative
is sarcocystis neurona or neospora hughesis the most common cause of EPM?
sarcocystis neurona
__ is where we prefer to start for treatment of EPM generally lasting __ weeks with __ toxicity. __ has a treatment period of __ months with many __ of treatment but is __. __ is similar to marquis with lower efficacy.
Marquis (ponazuril) is where we prefer to start for treatment of EPM generally lasting 6-8 weeks with no toxicity. SDZ/PYR has a treatment period of 4 months with many side effects of treatment but is cheaper. Diclazuril is similar to marquis with lower efficacy.
t/f: there is a vaccine for EPM
F
